Based on experiments in head-restrained animals, past studies have implicated a role for many cortical and subcortical regions in the control of saccadic eye movements. Neurons in the superior colliculus, for example, have since been investigated during head-free gaze shifts actually and were found to exhibit discharge properties that are correlated better with the coordinated eye-head movements than just the ocular component. Since the eyes and the head provide independent means of changing orientation, how does one gaze signal control movements of both? Is the gaze signal decomposed into eye and head components since different motor neurons innervate extraocular and neck muscles? If so, where and how does this decomposition occur? Is the accuracy of gaze shifts maintained by feedback mechanisms that monitor the coupled or independent contributions of the eyes and head? As higher structures have already been shown to code gaze, a bottom-up approach must be used to search for potential site(s) of decomposition of gaze. The aims of this proposal are, therefore, to study the contributions of brainstem burst, tonic, pause and motoneurons to gaze shifts. Specifically, the neural activity of these cells will initially be recorded during gaze shifts (head-free condition) and saccades (head-restrained condition) of equal amplitude, while systematically varying initial eye position. Then, the activity in these neurons will be altered by microstimulation and chemical microinjections. This latter experiment serves to perturb the oculomotor system and measure the accuracy maintained by its feedback mechanisms. A functional understanding of how a desired gaze signal results in a coordinated eye-head movement will consequently provide insights into potential circuitry malfunctions in patients with neurological disorders of the oculomotor system.